1. Field of the Invention
The present invention relates to detecting a site of origin of a natural electrical pulse inside a living body, such as a ventricular tachycardia arrhythmia (VT).
2. Description of the Related Art
Sudden cardiac death (SCD) afflicts an estimated 450,000 people annually in United States alone. Ninety percent of these events are related to structural heart disease, of which ischemic heart disease represents the majority. Loss of functioning myocardium through infarction leads to a decline in ventricular function and congestive heart failure, and provides the substrate for malignant ventricular tachyarrhythmias.
The recognition that depressed left ventricular systolic function secondary to myocardial infarction dramatically increases the risk of SCD led to the design and execution of several, large, multicenter, randomized trials over the past 15 years the results of which collectively showed a survival benefit conferred by the implantation of an implantable cardioverter-defibrillator (ICD) compared to optimal medical therapy alone. The ICD is now indicated for the primary prevention of SCD in patients with depressed left ventricular systolic function and symptoms of heart failure, and for secondary prevention in patients who have been resuscitated from an episode of SCD.
Ventricular tachycardia (VT) is a frequently-lethal arrhythmia arising from the ventricles that is most commonly associated with cardiac disease, mainly ischemic heart disease and idiopathic cardiomyopathy. With the advent and widespread use of the ICD, many patients are successfully treated for such malignant ventricular tachyarrhythmias, which would have been otherwise fatal. However, as such patients survive these events, both the incidence and prevalence of patients with recurrent ICD shocks for VT are increasing. Strategies to control VT include anti-arrhythmic medications and ablative therapy. The findings of the classic drug trials, specifically CAST, where anti-arrhythmic drugs were administered to suppress complex ventricular ectopy in post-myocardial infarction patients, were disturbing. Such drugs, namely the class I anti-arrhythmic drugs, were associated with increased, not decreased, mortality. It is now contraindicated to use this class of drugs in patients with structural heart disease. Therefore, there is a restricted choice of anti-arrhythmic drugs to use, with limited efficacy and considerable side effect profiles, in an increasing population of patients with VT who are receiving recurrent ICD shocks. Trial results have shown that ICD shocks are associated with increased patient morbidity, hospitalizations, and mortality.
The mechanical interruption of VT circuits in the left ventricular myocardium was first practiced by surgeons guided by cardiac electrophysiologists as subendocardial resection of scarred tissue and aneurysmectomy. Catheter-based techniques soon evolved, due to increasing demand. Currently the ablation of VT is almost solely performed in the electrophysiology laboratory by a cardiac electrophysiologist using a variety of energy sources, such as chemical, thermal, electrical and optical, and mainly by radiofrequency waves and low-temperature (cryo-ablation). However, myriad factors contrive to make catheter ablation of VT the most challenging electrophysiologic al procedure for a patient to undergo and an electrophysiologist to undertake. In its current state, catheter ablation for VT is indicated as important adjunctive therapy in patients with symptomatic VT in combination with the ICD and anti-arrhythmic drugs.
The most time-consuming step in the VT ablation procedure is the identification of its site of origin (SO). Considerable experience is required to conduct the rapid visual inspection and comparison of multiple electrocardiographs (ECGs) followed by rapid catheter manipulation to successive sites during pace-mapping. In pace-mapping, a stimulated electric pulse is introduced to the myocardium at a specific site using a catheter and the depolarization pulse propagation is monitored on 12 leads of a standard ECG. Automated matching of pace-maps and the VT ECG can be performed by existing software to determine when the myocardium has been stimulated at the VT SO. But, when the myocardium is stimulated at a site other than the VT SO, the matching software provides no data on the VT SO or any guidance as to where to stimulate or otherwise direct attention next to bracket or converge on the VT SO. Currently, there is no available automated technique that would guide the operator toward the VT SO.